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local anaesthesia Flashcards

1
Q

what is a local anaesthetic?

A

they are non-selective modifiers of neuronal function
-ie. they block action potentials in all neurons they have access to

selectivity/local effect is achieved by delivering LA to a limited area

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2
Q

what is a possible mechanism of action of LAs?

A
  • blocking/ inactivation of Na+ channels
  • hence preventing Na+ ion entry into cells
  • resulting in slowing down/complete halting of conduction
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3
Q

how does lipid solubility affect LA action?

A

higher lipid solubility -> higher potency and duration of action

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4
Q

what are some LAs with higher lipid solubility?

A

tetracaine (ester),
etidocaine, bupivacaine (amides)

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5
Q

what are some LAs with lower lipid solubility?

A

procaine (esters),
lidocaine, mepivacaine (amides)

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6
Q

how do the features of nerves affect their susceptibility to blockage by LAs?

A

nerves that are more susceptible to LAs blocks are:
- smaller
- myelinated
- sensory nerves (have higher frequency of firing)
- circumferential (instead of deep large nerve trunks)

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7
Q

what types of transmissions are blocked first by LAs?

A

nociceptive, sympathetic

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8
Q

how does pH affect LA activity?

A
  • higher pH (more alkaline environment) -> less proportion of ionised molecules -> INCREASE in LA potency

-note: LAs are generally weak bases, at physiological pH (7.35-7.45)- mostly but not completely ionised
- also: LAs work from WITHIN the cells, so they have to pass through the nerve sheath and axon membranes first before they exert their effects on the INTERNAL end of the sodium channels

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9
Q

what are the 2 types of LAs?

A
  • ester
  • amide
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10
Q

name 4 ester-type LAs

A

cocaine
procaine
tetracaine
benzocaine

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11
Q

name 5 amide-type LAs

A

lidocaine
mepivacaine
bupivacaine
etidocaine
prilocaine
ropivacaine

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12
Q

which LA is the least potent?

A

cocaine

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13
Q

what is the most potent ester type LA? what is its relative duration of action?

A

tetracaine (16)
long duration of action

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14
Q

what are the most potent amide type LAs?

A

bupivacaine, etidocaine, ropivacaine (16)
all: long duration of action

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15
Q

rank the relative potencies of ester LAs (cocaine ,procaine, tetracaine)

A

procaine (1) -> cocaine (2) -> tetracaine (16)

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16
Q

rank the relative potencies of amide LAs

A

mepivacaine (2) -> prilocaine (3) -> lidocaine (4) -> bupivacaine, etidocaine and ropivacaine (16)

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17
Q

what is/are some LA(s) with short duration of action?

A

procaine

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18
Q

what are some LAs with medium duration of action?

A

cocaine, lidocaine, mepivacaine, prilocaine

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19
Q

what are some LAs with long duration of action?

A

tetracaine, bupivacaine, etidocaine, ropivacaine

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20
Q

what are the differences between ester-type and amide-type LAs?

A
  • bond: ester bond vs amide bond
  • metabolism: esters by esterases in the plasma, vs amides by hepatic enzymes (esp. CYP450)
  • incidence of allergic reaction: low incidence for esters, very low for amides

note: allergic reactions caused by esters are due to ester LAs being hydrolysed into PABA (para-aminobenzoic acid) derivatives

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21
Q

what is the main cause of allergic reactions to ester LAs?

A

due to ester LAs being hydrolysed into PABA (para-aminobenzoic acid) derivatives

22
Q

how are ester-type LAs metabolised and excreted?

A

metabolised by non-specific esterases in the plasma/ tissues

metabolites excreted via urine

23
Q

how are amide-type LAs metabolised and excreted?

A

metabolised by hepatic enzymes (incl. CYP450)

metabolites excreted via urine

24
Q

why may epinephrine be administered together with LAs?

A
  • epinephrine -> causes vasoconstriction of surface vessels -> hence can prevent LA systemic distribution from the site of action

this may be used to:
- reduce risk of systemic toxicity
- minimise bleeding
- prolong duration of action of LAs at site of action by delaying systemic absorption

25
Q

when would you administer epinephrine with LAs?

A
  • if there large doses/concentrations of LA are required -> epi helps to reduce systemic absorption, to maintain therapeutic levels at site of action while reducing risk of systemic toxicity
  • to minimise bleeding
  • if prolonged anaesthesia is required (since delays systemic absorption -> extends duration of action of local anaesthetics -> reduce need for repeated dosing)
26
Q

when should epinephrine not be used with LAs?

A

if patient has:
- peripheral vascular disease/compromised blood supply (since vasoconstiction -> may cause peripheral ischaemia)
- cardiovascular concerns (esp: severe hypertension, CAD, arrhythmias, since vasoconstriction -> may lead to increase HR, BP, or cardiac arrhythmias
- allergy/sensitivity
- paediatric patients (since increased sensitivity to CVS effects of epi)

27
Q

what is the most cardiotoxic LA?

A

bupivacaine (amide)

28
Q

how can systemic toxicity arise from LA use?

A
  • unintended large dose of LA injected IV/intra-arterially accidentally -> immediate signs and symptoms of toxicity
  • overdose of LA injected locally -> absorption -> leads to high and toxic blood level -> later onset of signs and symptoms of toxicity
29
Q

what are some signs and symptoms of systemic LA toxicity?

A
  • CVS signs: cardiac contraction, arteriolar dilation, hypotension (extreme-> cardiovascular collapse)
  • CNS signs: sleepiness, visual and auditory issues, restlessness, nystagmus, shivering, convulsions, stopping of vital functions (extreme -> death)
30
Q

what is a possible consequence of cocaine usage? why?

A
  • hypertension
  • cocaine: blocks NE reuptake -> increase NE concentration -> vasoconstriction
31
Q

when is the vasoconstrictive effects of cocaine useful?

A
  • cocaine: gives good penetration and vasoconstriction -> used for ear, nose and throat procedures (ENT)

MOA- cocaine: blocks NE reuptake -> increase NE concentration -> vasoconstriction

32
Q

what is a danger of using prilocaine?

A
  • metabolite of prilocaine: O-toludine
  • can cause methaemoglobin (haemoglobin cannot bind to O2 properly -> can lead to bluish/purplish colouring of skin)
33
Q

what is the only route of administration for benzocaine? why?

A

only for surface use (topical)
- as it is very low solubility, hence used as a dry powder

34
Q

what drugs can be used for surface anaesthesia?

A

lidocaine
tetracaine
benzocaine

35
Q

what are some uses of surface anaesthesia?

A

nose, mouth, bronchial tree (spray), cornea, urinary tract

36
Q

what are considerations for drugs used for surface anaesthesia?

A

requires rapid penetration of the skin/mucosa, and limited tendency to diffuse away

37
Q

what is a risk of surface anaesthesia?

A

risk of systemic toxicity if high concentrations and large areas are involved

38
Q

what drugs are used for infiltration anaesthesia?

A

most LAs, often with addition of epinephrine

39
Q

what are some uses of infiltration anaesthesia?

A

minor surgeries
(since direct injection into tissues -> to reach nerve branches and terminals)

40
Q

what is a strong consideration and risk of infiltration anaesthesia?

A

only suitable for small areas
otherwise have serious risk of systemic toxicity!

41
Q

what drugs are used for nerve-block anaesthesia?

A

most LAs

42
Q

what are some uses of nerve-block anaesthesia?

A

surgery, dentistry, analgesia

LA injected close to nerve trunks -> loss of sensation peripherally

43
Q

what are some things to note for nerve-block anaesthesia?

A
  • less LA required than infiltration anaesthesia
  • accurate placement of needle is important!
  • slow onset
  • can use epi for vasoconstriction
44
Q

what drugs are used for epidural anaesthesia?

A

lidocaine, bupivacaine

45
Q

what are some uses of epidural anaesthesia?

A

spinal anaesthesia, for painless childbirth

LA injected into epidural space -> blocks spinal roots

46
Q

what are some things to take note of for epidural anaesthesia?

A

postoperative urinary retention is common!

47
Q

what is the definition of potency?

A

the dose required for 50% of people to experience the desired therapeutic effect

48
Q

what comorbidities/conditions would you look out for before prescribing certain LAs?

A
  • hepatic dysfunction -> avoid amide-types or adjust dosage (since amide-type LAs are metabolised by liver)
  • allergies to PABA (derived when esters are hydrolysed)
  • certain DDIs - CYP inhibitors/activators (since amide-types are largely metabolised by CYP enzymes)
49
Q

what are some things that inhibit CYPs and may cause adverse DDIs with amide-type LAs?

A
  • CYP inhibitors: grapefruit juice, cimetidine (H2 blocker), antibiotics (macrolides- erythromycin, etc.), antidepressants (SSRIs - fluoxetine, fluvocamine)
  • inhibition of CYPs -> decrease breakdown of amides -> increase concentration (so potency and duration affected, need to adjust dose accordingly)
50
Q

what are some things that induce CYPs and may cause adverse DDIs with amide-type LAs?

A
  • CYP inducers: St. John’s Wort, tabacco smoke, rifampin (anti-TB), carbamazepine
  • increase breakdown of amide-type LAs -> may result in lower efficacy -> may need to increase dose

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